The broad long-term objective is to provide first time data on the behavioral effects of melatonin uses a neuroprotective agent in a improved model of hypoxia-induced amnesia (HIA) in animals by isolating the effects on short-term from long-term memory in both young and aged subjects. In addition, assays of brain homogenates will offer melatonin's specificity of neuroprotection in the brain. These data are important because of their possible relevance to true clinical populations. If melatonin is to be considered an anti-oxidative therapy in the treatment of disease related free radical formation, it must first be determined that in vivo and in vitro results translate to real behavioral changes and how these behavioral changes are altered in older organisms. Furthermore, understanding melatonin's mode of protection, "what is its specificity in the brain) may guide the possible treatment strategy in the application of melatonin in not only the treatment of hypoxia-induced damaged, but to other neurodegenerative disease that commonly affect older adults and sometimes prematurely affect young adults.